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Mitochondrial Complex I Dysfunction and Peripheral Chemoreflex Sensitivity in a FASTK-Deficient Mice Model.

Angela Gomez-Niño1,2, Inmaculada Docio3,4, Jesus Prieto-Lloret3,4

  • 1Departamento de Biologia Celular, Histologia y Farmacologia/IBGM, Universidad de Valladolid-CSIC, Valladolid, Spain. angela@biocel.uva.es.

Advances in Experimental Medicine and Biology
|October 26, 2018
PubMed
Summary
This summary is machine-generated.

Mitochondrial Complex I is not essential for oxygen sensing in carotid bodies. Studies in FASTK knockout mice show normal respiratory responses to hypoxia, indicating Complex I

Keywords:
Carotid body chemoreceptorsComplex I. FASTK family proteinsMitochondria

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Area of Science:

  • Cellular Physiology
  • Mitochondrial Biology
  • Respiratory Control

Background:

  • The precise molecular mechanisms of oxygen sensing by carotid body (CB) chemoreceptors are not fully understood.
  • Mitochondria, particularly the electron transport chain (ETC), are implicated in CB oxygen sensing due to sensitivity to ETC blockers.
  • Reactive oxygen species (ROS) generated by the ETC are proposed mediators of oxygen sensing.

Purpose of the Study:

  • To investigate the role of mitochondrial Complex I in oxygen sensing by the carotid body.
  • To test the hypothesis that Complex I is essential for O2-sensing structures.
  • To study the effects of hypoxia on FASTK knockout mice, which have impaired Complex I biogenesis.

Main Methods:

  • Generation and study of FASTK knockout (FASTK-/-) mice with reduced Complex I activity.
  • Assessment of ventilatory responses to acute hypoxia and hypercapnia.
  • Measurement of carotid body catecholaminergic activity and hypoxic pulmonary vasoconstriction.
  • In vitro pulmonary artery contractility studies using small vessel myography.

Main Results:

  • FASTK knockout mice exhibited normal ventilatory sensitivity to hypoxia and hypercapnia compared to wild-type mice.
  • Carotid body catecholaminergic activity and hypoxic pulmonary vasoconstriction responses were similar in both groups.
  • Pulmonary artery vessels from knockout mice showed reduced relaxation to rotenone, an Complex I inhibitor.

Conclusions:

  • Complete functional Complex I, specifically the ND6 subunit, is not required for respiratory chemoreflex under hypoxic and hypercapnic conditions.
  • The study suggests alternative pathways or compensatory mechanisms are involved in carotid body oxygen sensing.
  • While Complex I function is affected, its complete absence does not abolish critical oxygen-sensing responses.